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BACKGROUND: Chronic spontaneous urticaria (CSU) is a skin disorder with an important immunologic profile. S100A8, S100A9, and S100A12 are the members of S100 family that have been reported to play important role in autoimmune diseases, but the characteristics of these three S100 members have not been defined in CSU. AIMS: This study was performed to investigate the levels of these three S100s in patients with CSU and to study whether they were associated with the severity and clinical characteristics of CSU. MATERIALS AND METHODS: The levels of plasma S100A8, S100A9, and S100A12 were measured in 51 CSU patients and 20 healthy controls using enzyme linked immunosorbent assay kits. The values in the patient group and that of the healthy controls were statistically compared. The relationships between the different markers were evaluated by correlation analysis. RESULTS: The plasma levels of S100A8, S100A9, and S100A12 were significantly higher in CSU patients than those in controls. Interestingly, the level of S100A12 was significantly correlated with S100A8 and S100A9 in CSU patients (P < 0.05 and P < 0.001, respectively). In addition, S100A8, S100A9, and S100A12 were all significantly inversely correlated with blood basophil percentage. CONCLUSIONS: Plasma S100A8, S100A9, and S100A12 levels were elevated in CSU patients. They might be useful biomarkers of CSU, with the potential role in the pathogenesis of CSU.

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OBJECTIVE: To investigate the mechanism of telomere shortening through 8-methoxypsoralen (8-MOP) and subsequent ultraviolet A (UVA) irradiation-induced photoaging model in human dermal fibroblasts (HDFs). METHODS: Photoaging model was established by 8-MOP + UVA in skin HDFs. Flow cytometer, enzyme cytochemistry, immunofluorescence, Western blot and Real-time PCR were employed. RESULTS: The percentage of G1 blockage of 8-MOP + UVA group were higher than that of control group at 24, 48, 72 h and 7 d (61.4% +/- 1.5% vs. 32.8% +/- 1.5%, 69.5% +/- 2.2% vs. 44.9% +/- 2.3%, 88.2% +/- 1.6% vs. 59.8% +/- 1.4%, 90.7% +/- 2.5% vs. 68.5% +/- 2.6%, all P < 0.01). The expression of SA-beta-Gal of 8-MOP + UVA group were higher than that of control group at 24, 48, 72 h and 7 d (34.87% +/- 0.59% vs. 7.11% +/- 0.78%, 59.38% +/- 0.46% vs. 10.57% +/- 0.47%, 72.46% +/- 0.98% vs. 11.67% +/- 0.87%, 94.33% +/- 0.13% vs. 12.04% +/- 0.12%, all P < 0.01). 8-MOP + UVA treatment could significantly aggravate the oxidative DNA damages, the percentage of 8-oxo-dG positive cell of 8-MOP + UVA group (95.78% +/- 0.14%) were significantly higher than that of control group (7.69% +/- 0.09%, P < 0.01), 8-MOP group (9.76% +/- 0.11%, P < 0.01) and UVA group (35.29% +/- 0.14%, P < 0.05). 8-MOP + UVA treatment could accelerate the telomere shortening ,the relative length of telomere of 8-MOP + UVA group were 2.57 +/- 0.05 lower than that of control group (6.63 +/- 0.12, P < 0.01). The levels of P53, P21(WAF-1) and P16(INK-4a) of 8-MOP + UVA group were higher than that of control group (3.00 +/- 0.88 vs. 0.54 +/- 0.10, 2.50 +/- 0.51 vs. 0.42 +/- 0.06, 2.21 +/- 0.34 vs. 0.38 +/- 0.05, all P < 0.01). CONCLUSION: 8-MOP + UVA-induced photoaging of HDFs can be mediated though the regulation of telomere and subsequent P53-dependent signaling pathways.

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BACKGROUND: Solar ultraviolet (UV) irradiation, in particular UVB with a wavelength range between 290 and 320 nm, induces different hazardous effects on the skin, including sunburn, photoaging and cancer. Protection against sun-induced damage is therefore a highly desirable goal. Chemoprevention is being investigated as a potential approach for the management of UV damages including skin cancer. AIM: In this study, to determine the relevance of our in vitro findings to in vivo situations, we assessed the effects of baicalin on UVB-mediated damages in mice skin. METHODS: Balb/C hairless mice were topically pretreated (24 h before UVB) or post-treated (5 min after UVB) with baicalin (1 mg/cm(2) skin area/mouse/100 microl acetone) and were exposed to UVB 24 h later (180 mJ/cm(2)). The animals were sacrificed 1 and 24 h after the UVB exposure. Skin edema, histopathology changes, hydrogen peroxide (H2O2) and cyclobutane pyrimidine dimers (CPDs)-positive cells were assessed to determine the UVB-induced photodamage. RESULTS: Our data demonstrated that a topical application of baicalin, either as a pretreatment or as a post-treatment, resulted in a significant decrease in UVB mediated increases in skin edema, skin hyperplasia and infiltration of leukocytes. Further, baicalin treatments (pre and post) also resulted in a significant decrease in UVB mediated (1) generation of H2O2 and (2) formation of DNA photolesions: CPDs. CONCLUSION: Based on these data, we suggest that baicalin could be developed as an agent for the management of conditions elicited by UV exposure including skin cancer.

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